A Comparative Analysis of Effect of Statins in Cardiovascular Patients on Root Canal Calcification Using CBCT: A Retrospective Study

Abstract

Objective

Root canal calcification (RCC) occurs as a diffuse phenomenon, making endodontic treatment challenging. Various factors like systemic diseases and medication induce the calcification process. It has been stated in studies that statin causes odontoblastic differentiation of human dental pulp stem cells, causing RCC. The objective of the study was to evaluate and compare RCC in healthy individuals and cardiovascular patients with and without statin therapy using cone-beam computed tomography (CBCT).

Materials and Methods

This retrospective study comprises three groups in which group 1 consisted of healthy individuals, group 2 consisted of cardiovascular patients not taking statin medication, and group 3 consisted of cardiovascular patients taking statin medication. The study included healthy first or second mandibular molar. CBCT was utilized to detect the RCC in terms of volume measurement among all the groups.

Statistical Analysis

For inferential analysis, a one-way analysis of variance and post hoc Tukey's test will assess the significance of sample means against known values.

Results

The pairwise comparison revealed that there is no significant difference between group 1 and group 2, and comparatively, group 3 significantly has higher calcification (least volume) than groups 1 and 2 in both mandibular first and second molar.

Conclusion

Systemic medications like statin possess an increased risk of RCC due to odontoblastic differentiation of human dental pulp stem cells. CBCT should be employed as a diagnostic tool for accurate diagnosis of RCC and correlating systemic oral illness and facilitating early diagnosis.

 

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Keywords

cardiovascular disease - cone-beam computed tomography - root canal calcification - statin

Introduction

The success rate of endodontic procedures has been reported to be as high as 95%. However, several factors continue to contribute to treatment failure. One such challenge is the presence of calcified canals that complicate the localization, cleaning, and shaping of root canals during endodontic therapy. Recent studies have demonstrated a strong correlation between statin use and root canal calcification (RCC). Statins are commonly used for their anti-inflammatory and antioxidant properties in patients with cardiovascular disease (CVD). The effect of systemic diseases like CVD and medication like statin on RCC has added a layer of complexity to endodontic diagnosis and treatment. This increases the risk of complications such as perforations and instrument separation. RCC results from the deposition of calcified tissue within the root canal, leading to partial or complete obliteration.[1] Multiple factors contribute to RCC, like dental trauma, aging, systemic conditions, and medications. RCC is closely associated with pulpal inflammation, which activates odontoblast-like cells and promotes secondary or tertiary dentin deposition.[2] Trauma from direct physical impact or chronic occlusal stress is a major cause of RCC. Aging leads to secondary dentin deposition, which naturally reduces pulp chamber and canal dimensions over time.

Systemic conditions such as CVDs, diabetes, and hormonal imbalances further accelerate calcification. Furthermore, medications like statins, particularly simvastatin, have been linked to increased calcification due to their effects on calcium metabolism and tissue mineralization.[3] RCC primarily affects molars due to their complex anatomy and exposure to occlusal forces. Emerging evidence suggests a strong correlation between RCC and CVD. Both conditions share underlying mechanisms of chronic inflammation and dysregulation of calcium-phosphorus metabolism.[4] Various diagnostic tools like intraoral periapical radiographs (IOPAs), bitewing radiographs, and cone-beam computed tomography (CBCT) have been used to identify RCC. While IOPA provides only a two-dimensional (2D) view, CBCT offers high-resolution and three-dimensional (3D) imaging. CBCT allows a comprehensive assessment of the extent of calcification, hence it is considered the gold standard for RCC diagnosis. There is a gap in the literature despite the increasing awareness of the association between RCC, systemic conditions, and medications like statins. Few studies have compared RCC in healthy individuals and cardiovascular patients on statins. Most research has focused on isolated factors without exploring the combined effects of systemic disease and medication-induced calcification. Additionally, the application of CBCT for RCC assessment in these groups remains underexplored. This study aims to fill these gaps by systematically evaluating and comparing RCC in healthy individuals and cardiovascular patients with and without statin therapy using CBCT. The findings will enhance our understanding of systemic–dental interactions and inform improved diagnostic and therapeutic strategies in endodontic practice.

 

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Materials and Methods

Sample Size

This retrospective study adhered to ethical guidelines and received approval from the Institutional Ethical Committee (IEC) of Manav Rachna Dental College, Manav Rachna International Institute of Research and Studies (MRIIRS/MRDC/SDS/IEC/2024/31). The STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) checklist and statement were meticulously followed, with a corresponding flowchart prepared to meet STROBE compliance ([Fig. 1]) ([Supplementary Material S1], online only).

Fig. 1 Flowchart of the study.

To determine the variation and difference in the volume, a pilot study was performed with the healthy and disease groups. Initially, the volume was calculated with 5 subjects of each group. The mean and standard deviation (SD) obtained in healthy was 1.35 (0.50) mL, considering this SD and a difference of 30% change in volume as clinically significant difference between the healthy and disease groups, we determined the Cohen effect size, which is closer to 0.4. We employed 25 subjects in each group for the present study as a sample of 22 in each group is sufficient with 80% power and 5% level of significance.

Sample size estimation was performed using G*Power software (version 3.0). With a study power of 80%, an effect size of 0.4, an α significance level of 0.05, and 2 degrees of freedom, the required sample size was calculated to be 75 participants, with 25 allocated to each group.

 

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Subjects

Participants were stratified into three groups: group 1 consisted of healthy individuals without systemic diseases or medications, group 2 included cardiovascular patients diagnosed for at least 5 years but not undergoing statin therapy, and group 3 comprised cardiovascular patients on statin therapy for at least 5 years. CBCT scans were retrieved from the PAPAYA 3D database and complemented by detailed medical and dental records. Confounding factors like tooth type (mandibular molars), age, gender, and systemic condition were matched carefully. The study included patients aged 30 to 45 years with first or second mandibular molars without significant pathology. Groups 2 and 3 participants must have at least 5 years of CVD diagnosis or statin use. The study only included patients with cardiovascular disorders; patients with other comorbidities or systemic conditions in which long-term medication was required were not included in the study to minimize the confounding variable and also to reach a conclusion that RCC is attributed to CVD with statin use.

Exclusion criteria included carious teeth, large restorations, attrition, periodontitis, prior pulp capping (vital pulp therapy), endodontic treatment, variable root canal anatomy, clenching or grinding habits, and systemic conditions such as diabetes mellitus, renal lithiasis, gout, or cholelithiasis, patients with other systemic diseases requiring medication, patients on multiple medications that are known to affect calcium metabolism like bisphosphonates and corticosteroids, and patients with early contact, that is, less than 5 years of history, were not included. Between January 2021 and March 2024, 91 CBCT scans were initially identified. After excluding 16 scans due to caries or radiographic periapical changes, 75 scans met the inclusion and exclusion criteria. Group 1 comprised 13 males and 12 females, group 2 included 14 males and 11 females, and group 3 consisted of 12 males and 13 females.

 

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Image Acquisition

CBCT was used for imaging, with scans sourced from the PAPAYA 3D database. The imaging parameters were set at 8.0 mA, 80 kV, 12 seconds of exposure, a slice thickness of 0.1 mm, and a slice interval of 1 mm. The voxel size was 100 µm for a detailed field of view. Images were reconstructed and analyzed in sagittal, coronal, and axial planes using the OnDemand 3D software. Oral radiologists with 10 years of experience underwent a blinded training session and interpreted the images.

 

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Image Segmentation

The OnDemand 3D software enabled segmentation and volumetric analysis of the root canal. Automatic segmentation with seed region growing was utilized, and the seed was placed within the root canal for reconstruction and was used to mark the boundary of the root canal. Threshold values were applied to define the lower (noncalcified regions) and upper (low-intensity surrounding dentin) limits. Voxels meeting these thresholds were included in the volumetric analysis. Segmentation was based on gray-level intensity distinctions in which the dentin appeared highly intense and pulp tissue less intense. Sagittal, coronal, and axial planes were marked to isolate the root canal. The delineated region corresponds to root canal configuration commonly observed as mesiobuccal (MB), mesiolingual (ML), distobuccal (DB), distolingual (DL), or distal. The pulp chamber floor was excluded to facilitate segmentation by separating it from the radicular pulp. A 3D reconstruction tool was employed to generate a 3D model of the root canal. The region of interest tool constrained segmentation boundaries to avoid the inclusion of coronal pulp voxels. Root canals were traced in all three planes ensuring accurate differentiation between MB, ML, DB, DL, or distal. The volume of the root canal was calculated after its reconstruction in three dimensions. A brief OnDemand 3D software workflow for root canal volume measurement has been added ([Fig. 2]).

Fig. 2 Brief OnDemand 3D software workflow for root canal volume measurement.

 

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Statistical Analysis

Data preprocessing included cleaning, reduction, and integration. Normality was assessed using the Shapiro–Wilk test and QQ plots. Descriptive statistics (mean ± SD) summarized demographic data. One-way analysis of variance (ANOVA) determined intergroup differences, followed by post hoc Tukey's test for pairwise comparisons. Exploratory data analysis utilized bar charts for visualization. All analyses were performed at a 5% significance level using Microsoft Excel and Python (Pandas, NumPy, Scipy). Findings were systematically interpreted to assess the impact of CVD and statin therapy on RCC.

 

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Results

A comprehensive one-way ANOVA was performed to ascertain statistically significant differences in RCC among the three study cohorts: (1) healthy individuals, (2) cardiovascular patients not undergoing statin therapy, and (3) cardiovascular patients receiving long-term statin treatment. The evaluation was conducted across distinct anatomical regions, including the MB, ML, DB, DL, and distal aspects of both the first and second mandibular molars. Significant intergroup variations were identified in the MB (p < 0.0001), ML (p = 0.0002), and distal (p = 0.0004) regions ([Table 1]). No statistically significant difference was noted for DB (p = 0.0520) and DL (p = 0.0886), as their p-values are greater than the level of significance ([Table 1]). Post hoc Tukey's test was performed for the multiple pairwise comparisons of the studied groups and revealed no statistically significant difference between group 1 and group 2 with a p-value of more than 0.05. Group 3 exhibited lower volume and hence markedly increased calcification levels compared with groups 1 and 2 (p < 0.05), suggesting the effects of statin therapy on calcific deposition within the root canal system ([Table 1]).

Table 1 Results of ANOVA and post hoc Tukey's test (first molar)

First molar	Group 1 healthy	Group 2 cardiovascular patient not taking any medication	Group 3 cardiovascular patient taking statin medication	One-way ANOVA F-test p-value	Group 1 vs. Group 2	Group 1 vs. Group 3	Group 2 vs. Group 3
MB	1.41 ± 0.45	1.33 ± 0.49	0.62 ± 0.43	0.0000[*]	0.8850	0.0000[*]	0.0000[*]
ML	1.41 ± 0.66	1.16 ± 0.64	0.51 ± 0.23	0.0002[*]	0.4280	0.0000[*]	0.0020[*]
DB	1.64 ± 0.57	1.35 ± 0.36	0.35 ± 0.00	0.0520	–	–	–
DL	1.51 ± 0.69	1.64 ± 0.00	0.34 ± 0.00	0.0886	–	–	–
Distal	1.59 ± 0.36	1.43 ± 0.51	0.77 ± 0.42	0.0004[*]	0.7760	0.0050[*]	0.0010[*]

Abbreviations: ANOVA, analysis of variance; DB, distobuccal; DL, distolingual; MB, mesiobuccal; ML, mesiolingual.

^* signifies - statistically significant difference with p-value < 0.05.

Post hoc Tukey's test was performed for multiple pairwise comparison and revealed statistically significant difference between Group 1 and 3, and Group 2 and 3. Group 3 exhibited lower volume and hence markedly increased calcification levels compared to Group 1 and 2 (p < 0.05).

The bar graph depicts mean calcification levels across the different anatomical regions illustrating a marked reduction in volume exhibiting higher calcification among statin users compared with the other two groups. Notably, while groups 1 and 2 exhibit decreased levels of calcification in most regions, group 3 consistently demonstrated significantly higher calcification, highlighting the systemic impact of statins on mineral deposition ([Fig. 3]).

Fig. 3 Graphical representation of first molar analysis depicting volume distribution across different anatomical regions of the root canal.

A parallel statistical analysis was conducted for the second mandibular molar to validate findings and assess whether the observed trends extended to adjacent dentition. Statistically significant differences were observed across the MB (p = 0.0001), ML (p = 0.0015), and distal (p = 0.0001) regions, which was similar to the pattern identified in the first molar analysis ([Table 2]). The DB and DL regions were notably absent in group 3 and were recorded in only a single case within group 2 ([Table 2]). As observed in the first molar, no significant differences were detected between groups 1 and 2 in the MB, ML, and distal regions (p > 0.05). Group 3 demonstrated significantly lower volume and, hence, higher calcification levels relative to groups 1 and 2 (p < 0.05) ([Table 2]).

Table 2 Results of ANOVA and post hoc Tukey's test (second molar)

Second molar	Group 1 healthy	Group 2 cardiovascular patient not taking any medication	Group 3 cardiovascular patient taking statin medication	One-way ANOVA F-test p-value	Group 1 vs. Group 2	Group 1 vs. Group 3	Group 2 vs. Group 3
MB	1.45 ± 0.49	1.50 ± 0.40	0.59 ± 0.23	0.0001[*]	0.9800	0.0000[*]	0.0020[*]
ML	1.29 ± 0.50	1.09 ± 0.42	0.55 ± 0.24	0.0015[*]	0.6570	0.0100[*]	0.0650
DB	0.92 ± 0.29	0.65 (single observation)	Not present	–	–	–	–
DL	0.81 ± 0.16	1.00 (single observation)	Not present	–	–	–	–
Distal	1.65 ± 0.41	1.43 ± 0.35	0.83 ± 0.22	0.0001[*]	0.5190	0.0000[*]	0.0210[*]

Abbreviations: ANOVA, analysis of variance; DB, distobuccal; DL, distolingual; MB, mesiobuccal; ML, mesiolingual.

^* signifies - statistically significant difference with p-value < 0.05.

As observed in the first molar, no significant difference was detected between Group 1 and 2 in MB, ML, and distal region. Post hoc Tukey's test was performed for multiple pairwise comparison and revealed statistically significant difference between Group 1 and 3, and Group 2 and 3. Group 3 exhibited lower volume and hence markedly increased calcification levels compared to Group 1 and 2 (p < 0.05).

The bar graph indicates that group 3 consistently exhibits significantly lower volume across the measured regions, demonstrating higher calcification in the statin group. The graphical representation demonstrates the correlation between statin use and RCC prevalence, specifically comparing groups 1 and 2 to group 3. The distribution patterns also suggest a consistent effect across different teeth, indicating the broader impact of statin therapy on dental mineralization ([Fig. 4]).

Fig. 4 Graphical representation of second molar analysis depicting volume distribution across different anatomical regions of the root canal.

We performed a t-test to evaluate whether there is any difference between the first and second molar in RCC. The t-test results reveal no statistically significant difference between the first and second molars across the various experimental parameters and within the three treatment groups, as all p-values exceed the significance level of 0.05 ([Table 3])

Table 3 First and second molar analysis across the various experimental parameters and within the three treatment groups

Treatment groups	Parameters	First molar	Second molar	Independent t-test, p-value
Group 1, healthy patients	MB	1.41 ± 0.45	1.45 ± 0.49	0.8334
	ML	1.41 ± 0.66	1.29 ± 0.50	0.5914
	DB	1.64 ± 0.57	0.92 ± 0.29	0.1362
	DL	1.51 ± 0.69	0.81 ± 0.16	0.2152
	Distal	1.59 ± 0.36	1.65 ± 0.41	0.7897
Group 2, cardiovascular patient not taking any medication	MB	1.33 ± 0.49	1.50 ± 0.40	0.5047
	ML	1.16 ± 0.64	1.09 ± 0.42	0.8222
	DB	1.35 ± 0.36	0.65 ± nan	nan
	DL	1.64 ± 0.00	1.00 ± nan	nan
	Distal	1.43 ± 0.51	1.43 ± 0.35	0.9984
Group 3, cardiovascular patient taking statin medication	MB	0.62 ± 0.43	0.59 ± 0.23	0.8795
	ML	0.51 ± 0.23	0.55 ± 0.24	0.7274
	DB	0.35 ± 0.00	nan ± nan	nan
	DL	0.34 ± 0.00	nan ± nan	nan
	Distal	0.77 ± 0.42	0.83 ± 0.22	0.6897

Abbreviations: DB, distobuccal; DL, distolingual; MB, mesiobuccal; ML, mesiolingual.

Note: nan, there we have only one observation, in that case we cannot apply any statistical tests.

Interoperator agreement analysis was performed, and based on the results of the independent t-test, there are no statistically significant differences in the molar parameters between the two examiners, as all p-values exceed the significance threshold of 0.05 ([Table 4]).

Table 4 Interobserver agreement analysis

Molar	Parameters	Examiner 1 (gives 37)	Examiner 2 (gives 38)	Independent t-test, p-value
First molar	MB	1.36 ± 0.47	0.99 ± 0.59	0.0512
	ML	1.27 ± 0.69	0.88 ± 0.59	0.0501
	DB	1.80 ± 0.78	1.18 ± 0.61	0.1981
	DL	1.45 ± 0.65	1.27 ± 0.79	0.7327
	Distal	1.46 ± 0.45	1.08 ± 0.58	0.0566
Second molar	MB	1.43 ± 0.55	1.05 ± 0.56	0.1111
	ML	1.31 ± 0.53	0.85 ± 0.46	0.0506
	DB	0.71 ± nan	0.89 ± 0.33	0.7415
	DL	0.70 ± nan	0.96 ± 0.06	0.1658
	Distal	1.50 ± 0.37	1.21 ± 0.54	0.1922

Abbreviations: DB, distobuccal; DL, distolingual; MB, mesiobuccal; ML, mesiolingual; nan, null value.

 

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Discussion

The objective of the study was to evaluate the effect on RCC among cardiovascular patients with or without statins using CBCT. Previously, multiple studies have been conducted evaluating pulp chamber calcification. One major limitation of these studies has been the 2D assessment, and none of them aimed to measure the RCC using 3-day volumetric analysis.[5] [6] [7] [8] Hence, to surpass these drawbacks, we conducted a study that measured RCC in a healthy group, cardiovascular patients not taking statin medication, and cardiovascular patients taking statin medication. In the present study, we have recruited cardiovascular patients taking statin medication for at least 5 years, this is because in a study it has been found that the coronary artery calcium score tends to increase with the duration of the therapy, hence to evaluate the effect caused by statin the minimum duration of therapy should be of 5 years.[9] To standardize this, we have recruited group 2 and group 3 patients with 5 years of history. Hence, early contact that is less than 5 years of history was not included.

We have selected an age range of 30 to 45 years because this includes patients in young to middle age, and the presence of other systemic disease is very less likely to be present, hence reducing the confounding variables and helps in establishing the direct effect of CVD or statin medication on RCC. Also, it has been stated in a study that with increasing age, there are chances of increasing cardiovascular mortality rate with unmodifiable risk factors; hence, it will not help us to reach the conclusion whether the effect is due to the disease or the medication.[10]

This retrospective study's findings indicate that long-term statin therapy is associated with significantly higher RCC compared with both healthy individuals and cardiovascular patients not on statins. This effect was consistently observed across multiple anatomical regions of the first and second mandibular molars. The results further demonstrate that while CVD alone does not appear to influence RCC, statin therapy plays a significant role in mineral deposition within the root canal. The lower volume of root canal and increased calcification observed in statin users highlights the systemic impact of these medications on dental tissues similar to existing literature suggesting that statins may promote mineralization. The present study performs volumetric analysis of individual root canals (MB, ML, DB, DL, or distal). Segmentation was done to evaluate the calcification in distinct canals for more precision and accurate results and to prevent the masking of the localized variations in calcification patterns. Also, the root canal configuration is not uniform within all canals; evaluating individual canals provides more clinically relevant findings. Edds et al found a significant association between preexisting CVD and pulp stones with a higher prevalence in teeth with noninflamed pulps.[5] Similarly, Khojastepour et al observed increased canal calcification rates in individuals with ischemic heart disease.[11] Srivastava et al noted a higher prevalence of pulp stones in cardiovascular patients over 50 years, particularly in first molars and the maxillary dentition.[6] Statins are commonly prescribed for lipid-lowering and cardioprotective effects and are known for their pleiotropic effects, anti-inflammatory properties, modulation of vascular endothelial function, and enhancement of osteoblastic activity via the bone morphogenetic protein 2 (BMP-2) pathway. Particularly, simvastatin has been shown to enhance mineralization by upregulating osteoblastic activity and promoting calcium deposition. These factors collectively contribute to increased mineralization in various tissues, including dental pulp, which has been discussed in various studies. A study by Okamoto et al demonstrated that simvastatin promoted mineralized tissue formation in dental pulp stem cells.[12] Pettiette et al found that statin use increased calcification and reduced vertical pulp chamber height in mandibular molars.[7] Bains et al observed a higher prevalence of coronal pulp stones in cardiovascular patients compared with those with cholelithiasis or renal lithiasis.[8] Further adding to this, Varalakshmi et al's findings suggest that simvastatin accelerated odontogenic differentiation in human dental pulp cells indicated by the expression of odontogenic markers like dentin sialophosphoprotein, dentin matrix protein-1, and BMP-2 and formation of mineralized nodules.[13] Another study by Leite et al suggests that simvastatin increases the metabolism and capability of odontoblasts to deposit a mineralized matrix.[14]

Even though RCC is often asymptomatic, it still poses a significant challenge in endodontic treatment. The deposition of tertiary dentin leads to circumferential narrowing of the root canals. This makes canal access, patency, and instrumentation difficult.[15] Failure to achieve patency to the apical third can compromise infection control, increasing the risk of procedural errors such as transportation, ledging, perforations, and instrument fractures. Such errors further reduce the prognosis by impairing the ability of a clinician to eliminate intracanal infection effectively, ultimately causing root canal treatment failure. Additionally, the increased torsional and bending forces required to instrument calcified canals increases the risk of iatrogenic damage, further reducing the treatment outcome.[16] Failure of treatment leads to prolonged procedures, increased discomfort, and a higher risk of complications. This can result in persistent pain, infection, or the need for more invasive interventions like tooth extraction. This study has highlighted the importance of history-taking in patients with CVD. Such patients must undergo pretreatment assessment using CBCT to analyze the extent of calcification. Using ultrasonic tips and specialized burs may allow conservative dentin removal while preserving the tooth structure. This must be followed by regular follow-ups and preventive dental care to improve patient prognosis.

The coronal pulp was excluded from the present study because earlier research had already been conducted to evaluate pulp chamber calcification. To independently evaluate the effect of calcification on root canals, this study specifically focused on the impact of CVD and statin therapy on RCC. The pulp chamber of mandibular molars contains the maximum cellular and vascular components and, hence, they are the first teeth to get exposed to any insult or any systemic condition impacting the oral cavity. If metabolic dysfunction occurs, the pulp chamber is the first where the calcification is initiated, followed by the root canal.[17]

Most of the studies evaluated pulp chamber calcification with CVD and statin therapy on 2D radiographs. A study by Pettiette et al[7] evaluated the correlation between statin and pulp chamber calcification and concluded that there was a significant increase in calcification and loss of vertical height in mandibular molar. Our previous study and a study by Srivastava et al[6] had already established the role of systemic disease on pulp chamber calcification using CBCT. Hence, no study till now has evaluated the role of systemic diseases or statin therapy on RCC. That is why the intent of this study was to independently focus on RCC.

This is the first study that independently evaluated the role of statin therapy on RCC. No study till now has evaluated the impact on RCC after systemic disease or systemic medication. Most of the studies evaluated the effect of statins or glucocorticoids on pulp chamber calcification. But none of them till now evaluated independently on root canals. A study by Pettiette et al states that long-term use of statins and glucocorticoids induces pulp obliteration.[7] Various other studies had also stated about pulp calcification and its etiological factors, but none of them researched independently on root canal using 3D volumetric analysis. Hence, this study is clinically relevant because it improved endodontic diagnosis and treatment planning, preventing procedural errors and correlating medical history with the patient's oral health and bridging the knowledge gap as atherosclerosis is a well-studied phenomenon that occurs in the innermost layer of arteries. However, its impact on RCC has never been studied. This study opens up a new path for more exploration and links between the systemic disease and dental pathology.

A small sample size, lack of longitudinal data, its retrospective design, and cardiovascular patients, for complete relief, do take other medications that may have an impact on calcium metabolism, inducing RCC; hence, polypharmaceutical may have an effect on RCC that was not considered in the present study are certain limitations of this study. A study with more robust data and a larger sample size will be required in the future to further establish this correlation between statin use and RCC. Future studies should also focus on a molecular-level assessment of key enzymes and signaling pathways involved in statin-induced RCC like BMPs and alkaline phosphatases to elucidate the precise mechanisms of odontoblastic differentiation and dentin mineralization. Additionally, more clinical outcome-based research should assess the success of endodontic treatment in statin users. Furthermore, prospective, longitudinal studies should evaluate whether prolonged statin therapy leads to progressive RCC and its impact on long-term tooth survival.

 

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Conclusion

This study provides evidence that systemic statin therapy is associated with increased RCC in cardiovascular patients. The significant differences observed across multiple root regions suggest a systemic influence of statins on odontogenic mineralization. These findings highlight the potential risk of statin therapy while diagnosing and treating RCC. Clinicians should employ advanced diagnostic tools and modified treatment strategies to optimize endodontic outcomes in patients with a long history of statin. Future research should focus on finding the molecular pathways linking statins to dental mineralization and exploring potential therapeutic interventions to mitigate excessive RCC in affected patients.

 

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Conflict of Interest

None declared.

Acknowledgment

The authors wish to acknowledge the services of Mr. Arjun Mane (Manav Rachna Dental College, MRIIRS) for the detailed statistical analysis.

Ethical Approval

This cross-sectional study was approved by the Institutional Internal Ethical Committee (IEC) of the School of Dental Sciences, MRIIRS, Faridabad (letter no. MRIIRS/MRDC/SDS/IEC/2024/31 dated 18.06.2024).

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Publication History

Article published online:
25 July 2025